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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased sympathetic activity seems to play an important role in the pathogenesis and development of complications of atherosclerotic origin in patients with essential hypertension (EH). The aim of this study was to evaluate the effect of a new antihypertensive agent, moxonidine (M), on microalbuminuria (urine albumin excretion, UAE), plasma thrombomodulin (TM), and tissue plasminogen activator inhibitor (PAI-1) in patients with mild to moderate EH associated with increased UAE. Fifty-eight patients (32 M, 26 F) with EH and microalbuminuria, with a mean age of 56.6 +/- 8.2 years and a body mass index (BMI) of 23.8 +/- 3.1 kg/m2 who responded to M therapy (0.3-0.4 mg/daily) were studied before and after their blood pressure control. The 24-hour urine albumin excretion (RIA method), as well as TM and PAI-1 plasma levels (ELISA method), were determined before and 6 months after the initiation of treatment under moxonidine therapy. At the end of the 6-month period, all patients remained normotensive. The 24-hour urine albumin excretion had decreased to 24.5 +/- 6.4 vs. 32.3 +/- 7.2 ug/min before therapy (P < 0.001). The plasma TM levels had decreased to 44.0 +/- 7 vs. 51.0 +/- 9 ng/mL before therapy (P < 0.01), and PAI-1 levels had also decreased to 11.5 +/- 4.5 vs. 15.8 +/- 8 IU/mL before therapy (P < 0.05). The results of our study suggest that in hypertensive patients with microalbuminuria, moxonidine, an imidazoline I1-receptor agonist, a new centrally acting antihypertensive agent, significantly reduces urine albumin excretion as well as thrombomodulin and PAI-1 levels. These preliminary findings demonstrate a favorable effect on renal function and endothelial homeostatic mechanisms (maintenance of haemostatic balance).
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PMID:Moxonidine effect on microalbuminuria, thrombomodulin, and plasminogen activator inhibitor-1 levels in patients with essential hypertension. 992 77

To better understand the links between circulating insulin and albuminuria in essential hypertension, the plasma insulin response t alpha a 75 gram glucose load and albuminuria were evaluated in 53 glucose-tolerant essential hypertensives and 12 controls. To allow any direct pressure-independent albuminuric effect of insulin to emerge more clearly, those same parameters were also evaluated in 20 glucose-tolerant normotensive patients with stable atherosclerotic peripheral vascular disease, a condition in which hyperinsulinaemia could be anticipated on the basis of previous reports. In response to glucose ingestion, hyperinsulinaemia was evident in both hypertensive and normotensive atherosclerotic patients, while, on average, urine albumin was elevated only in the former. When plasma insulin, systolic and diastolic blood pressure (BP) (by 24-h ambulatory BP monitoring), plasma glucose, triglycerides and body mass index were entered into a multiple regression analysis, only systolic BP appeared to exert an independent effect on urine albumin. Post-glucose load plasma insulin did not differ between hypertensive patients with (n = 14) and without (n = 39) microalbuminuria (albuminuria > 20 micrograms/min). In further analyses, insulin and systolic BP values were divided in quartiles: albuminuria did not differ across insulin quartiles, while it was significantly higher in the top (n = 21) vs the bottom (n = 21) systolic BP quartile. Thus, hyperinsulinaemia and microalbuminuria were unrelated variables in these hypertensive and atherosclerotic patients. Blood pressure, particularly systolic, emerged as a primary predictor of urinary albumin excretion, although the importance of this parameter needs to be proved prospectively.
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PMID:Dissociation between albuminuria and insulinaemia in hypertensive and atherosclerotic men. 1010 62

BACKGROUND: Microalbuminuria, a marker of early renal damage, predicts mortality in non-diabetic subjects. The loss of circadian blood pressure regulation is associated with the severity of essential hypertension and has been reported in hypertension due to renal disease. We therefore looked for a possible link between microalbuminuria and the smaller decrease in nocturnal blood pressure that occurs in essential hypertension.METHODS: The 24 h ambulatory blood pressure of 52 subjects with essential hypertension was measured and their urine tested for microalbuminuria (urinary albumin excretion of 30-300 mg/24 h). RESULTS: The subjects with (n = 10) and without (n = 42) microalbuminuria were comparable in clinical characteristics, antihypertensive treatments and serum creatinine. They had significantly different night-time systolic, diastolic and mean blood pressure decreases on ambulatory blood pressure monitoring. Two-factor analysis of variance showed that the day-night blood pressure decrease was linked to microalbuminuria status. The day-night blood pressure change of subjects with microalbuminuria differed from that of subjects without microalbuminuria independently from the daytime blood pressure level. CONCLUSION: Subjects with essential hypertension and microalbuminuria show a loss of nocturnal blood pressure decline. Whether microalbuminuria indicates a subtype of essential hypertension due to renal disease or severe hypertension with early renal damage remains to be clarified.
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PMID:Loss of the nocturnal decline in blood pressure in subjects with essential hypertension and microalbuminuria. 1022 77

1. Both microalbuminuria and left ventricular hypertrophy may reflect target organ damage in essential hypertension. Both are related to the prevailing level of blood pressure and both are associated with an increase in morbidity and mortality. 2. The database of the Hypertension Diagnostic Service, a multicentre secondary referral clinic for patients with essential hypertension, was analysed in order to clarify the level of association between microalbuminuria and left ventricular hypertrophy, which might explain the observed increase in morbidity and mortality in patients with microalbuminuria. Microalbuminuria was measured semiquantitatively by urine dip-stix. After the exclusion of patients with potential secondary hypertension, renal disease and diabetes mellitus, patients with complete data for microalbuminuria, left ventricular mass (LVM) and 24 h blood pressure monitoring were selected. 3. Data were complete for 704 patients (47% male, age 51 +/- 12 years) and 42% tested positive for microalbuminuria. Microalbuminuria was positively related to 24 h systolic blood pressure and weight and was negatively related to age. Left ventricular mass was higher in patients with microalbuminuria (men, 265 +/- 69 g; women, 207 +/- 61 g) than in those without (men, 250 +/- 64 g, P < 0.05; women, 185 +/- 50 g, P < 0.001). After correction for the effects of gender, body mass index and 24 h systolic blood pressure, the presence of microalbuminuria was associated with an increase in LVM of 10 g (P < 0.05, 95% confidence interval, 2-19 g).
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PMID:Left ventricular mass and microalbuminuria: relation to ambulatory blood pressure. Hypertension Diagnostic Service Investigators. 1040 76

Urinary excretion of albumin exceeds normal values in 10 to 25% of patients with essential hypertension. The level of albuminuria is highly correlated with arterial pressure, and more closely with ambulatory arterial pressure. The interaction between albuminuria and arterial pressure is enhanced by overweight, smoking, protein intake, insulin resistance, lipid abnormalities, and possibly genotypes of the components of the renin-angiotensin system. The renal mechanisms of microalbuminuria are not well elucidated. Notably, an increase in filtration fraction suggestive of intraglomerular hypertension was observed in patients with hyperfiltration. Microalbuminuria may be a marker of diffuse vascular abnormalities predisposing to cardiovascular disease and/or hypertensive renal disease heralding future renal failure, but its predictive value needs to be tested in more long-term follow-up studies. Antihypertensive treatment has a varied influence on albuminuria; angiotensin-converting enzyme inhibitors may correct this abnormality (at least partially) better than other agents.
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PMID:Microalbuminuria in essential hypertension. 1045 69

Microalbuminuria (an increased urinary albumin excretion that is not detectable by the usual dipstick methods for macroproteinuria) predicts cardiovascular events in essential hypertensive patients. A possible reason for this behavior is that albumin leaks through exaggeratedly permeant glomeruli exposed to the damaging impact of subclinical atherogenesis. To evaluate this possibility, the transcapillary escape rate of albumin (TER(alb), the 1-hour decline rate of intravenous (125)I-albumin), a parameter that estimates the integrity of systemic capillary permeability, albuminuria, blood pressure, echocardiographic left ventricular mass, lipids, and body mass index were measured in 73 uncomplicated, glucose-tolerant men with essential hypertension and normal renal function; 53 were normoalbuminuric, and 20 were microalbuminuric. Twenty-one normotensive age-matched male subjects were the controls. TER(alb) was higher in hypertensives, a behavior explained in part by a positive correlation with blood pressure values, although body mass index, lipids, and left ventricular mass showed no association. Transcapillary albumin leakage values did not differ between normoalbuminuric and microalbuminuric patients and were unrelated to albuminuria. Blood pressure, particularly systolic, and cardiac mass were higher in microalbuminuric patients in whom albuminuria correlated with both cardiovascular variables and indicated the influence of the hemodynamic load on urinary albumin levels. Thus, TER(alb), a parameter influenced by the permeability surface area product for macromolecules and the filtration power across the vascular wall, is altered in essential hypertensives. However, this abnormality is dissociated from the amount of albuminuria, which is contrary to the hypothesis that a higher albumin excretion reflects a greater degree of systemic microvascular damage in essential hypertension.
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PMID:Microalbuminuria and transcapillary albumin leakage in essential hypertension. 1048 99

Endothelin-1 (ET-1) as a potent vasoconstrictor, has mitogenic and inotropic properties, stimulates the renin-angiotensin-aldosterone system and sympathetic nervous system. The results of recent studies suggest that overall hemodynamic effects of ET-1 may play a part in the control of blood pressure and the pathophysiology of hypertension. Several investigators have invoked increase level of ET-1 in human essential hypertension but the results of studies concerning hypertensive patients with normal renal function have shown that they have similar concentrations of ET-1 to those in normotensives. To establish whether ET-1 may elevate of blood pressure, the value of plasma ET-1 activity was determined in peripheral blood in 101 patients with essential hypertension. There was no significant difference between in mean level of ET-1 in patients with essential hypertension and in control group. The plasma ET 1 was significantly higher in patients with severe hypertension than that of patients with mild and moderate hypertension, and in patients with severe hypertension there was a correlation between the level of ET-1 and microalbuminuria. There was no correlation between the plasma ET-1 level and systolic blood pressure and diastolic blood pressure in the patients with essential hypertension as a whole, not was there any correlation between ET-1 and noradrenaline, aldosterone level and renin plasma activity.
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PMID:[The level of plasma endothelin-1 in patients with essential hypertension]. 1052 17

Some patients with essential hypertension manifest greater than normal urinary albumin excretion (UAE). The significance of this association, which is the object of this review, is not well established. Hypertensive patients with microalbuminuria manifest greater levels of blood pressure, particularly at night, and higher serum levels of cholesterol, triglycerides, and uric acid than patients with normal UAE. Levels of high-density lipoprotein cholesterol, on the other hand, were lower in patients with microalbuminuria than in those with normal UAE. Patients with microalbuminuria manifested greater incidence of insulin resistance and thicker carotid arteries than patients with normal UAE. After a follow-up of 7 years, we observed that 12 cardiovascular events occurred among 54 (21.3%) patients with microalbuminuria and only two such events among 87 patients with normal UAE (P < 0.0002). Stepwise logistic regression analysis showed that UAE, cholesterol level, and diastolic blood pressure were independent predictors of the cardiovascular outcome. Rate of creatinine clearance from patients with microalbuminuria decreased more than that from those with normal UAE. In conclusion, these studies suggest that hypertensive individuals with microalbuminuria manifest a variety of biochemical and hormonal derangements with pathogenic potential, which results in hypertensive patients having a greater incidence of cardiovascular events and a greater decline in renal function than patients with normal UAE.
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PMID:Microalbuminuria in essential hypertension: significance, pathophysiology, and therapeutic implications. 1058 27

Whether microalbuminuria (MA) is the result of intrarenal hemodynamic changes induced by increased systemic blood pressure (BP) or a marker of capillary leakiness at the glomerular level that reflects more generalized atherosclerotic vascular damage is still debated. To address this question, 319 patients without diabetes, 154 men and 165 women aged 57 +/- 8.6 years (range, 37 to 73 years), but with essential hypertension (EH) never treated with drugs were enrolled onto the study. Using a multiple linear regression analysis, we analyzed the prevalence of MA and its relationship with BP level as well as with other risk factors for the development of atherosclerosis. MA was present in 40% of the population studied. A univariable analysis of ambulatory BP monitoring measurements showed that only 24-hour systolic BP (P = 0.04), daytime systolic BP (P = 0. 02), and 24-hour daytime and nighttime systolic BP load (P < 0.01) predicted the presence of MA, whereas all BP variability parameters significantly predicted it. Multivariable analysis showed that only a positive family history of hypertension (P < 0.001), BMI (P < 0. 001), glucose (P < 0.001), and 24-hour systolic BP coefficient of variation (P < 0.001) independently predicted MA. In summary, the prevalence of MA in our group of patients with EH was high, presumably as a consequence of the older mean age of the population and the selection criteria. Besides being a marker of concomitant cardiovascular damage, MA was associated with a worse pattern of atherosclerotic risk factors. Although its pathophysiological meaning remains to be completely clarified, MA seems to be more related to other atherosclerosis risk factors and presumably reflects a more diffuse vascular injury.
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PMID:Atherosclerosis profile and microalbuminuria in essential hypertension. 1058 27

To identify the biological covariates of microalbuminuria (albuminuria >/=15 microg/min) in nondiabetic subjects, brachial blood pressure, echocardiographic left ventricular mass, and other cardiovascular and metabolic parameters were evaluated in 211 untreated males (38 normal controls, 109 uncomplicated stage 1 to 3 essential hypertensives, and 64 patients with clinically stable atherosclerotic peripheral vascular disease either with [n=44] or without [n=20] essential hypertension) with normal cardiac and renal function. Compared with normoalbuminuric subjects, microalbuminuric subjects (n=67) were characterized by higher systolic blood pressure, comparable diastolic blood pressure, and, therefore, wider pulse pressure. Greater prevalence of hypertension, peripheral vascular disease, left ventricular hypertrophy, and reduced HDL cholesterol values further distinguished microalbuminuric from normoalbuminuric subjects in univariate comparisons. The risk of microalbuminuria increased by ascending pulse pressure quintiles in age-corrected logistic regression models, in which pulse pressure was more predictive than systolic pressure and was independent of mean pressure. When microalbuminuric status was regressed against a series of dichotomous (vascular and active smoker status) and continuous (age, pulse and mean pressure, left ventricular mass index, and HDL and LDL cholesterol) variables, only pulse pressure, left ventricular mass index, and smoking status were independent predictors. The association of increased albuminuria with wider pulse pressure, a correlate of the pulsatile hemodynamic load and conduit vessel stiffness as well as an important cardiovascular risk factor, may explain why microalbuminuria predicts cardiovascular events in nondiabetic subjects. The independence from concomitant vascular disease also suggests that wider pulse pressure, rather than representing a simple marker for atherosclerotic disease, influences albuminuria directly.
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PMID:Microalbuminuria and pulse pressure in hypertensive and atherosclerotic men. 1064 74


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